Endoscopic submucosal dissection for the treatment of early Barrett’s neoplasia: long-term outcomes of a prospective multicenter study

Guillaume Bergez^a, Vincent Lépilliez^b, Thierry Ponchon^c, Mathieu Pioche^c, Jérome Rivory^c, Timothée Wallenhorst^d, Emmanuel Coron^e, Nicolas Chapelle^e, Jérémie Jacques^f, Romain Legros^f, Pierre Deprez^g, Enrique Perez Cuadrado Robles^g, Arthur Berger^h, Edouard Chabrun^h, Geoffroy Vanbiervlietⁱ, Stanislas Chaussade^a, Sarah Leblanc^a, Romain Coriat^a, Frédéric Prat^a, Maximilien Barret^a

Hôpitaux de Paris, France; Edouard Herriot Hospital, Hospices Civils de Lyon, France; Jean Mermoz Private Hospital, Ramsay Santé; Dupuytren Hospital, Limoges, France; University Hospital of Bordeaux, France; University Hospital of Nice, France; University Hospital of Nantes, France; University Hospital of Rennes, France; University Clinics of Saint Luc, Brussels, Belgium

^aDepartment of Gastroenterology and Digestive Oncology, Cochin Hospital, Assistance Publique, Hôpitaux de Paris, France (Guillaume Bergez, Stanislas Chaussade, Sarah Leblanc, Romain Coriat, Frédéric Prat, Maximilien Barret); ^bDepartment of Gastroenterology, Jean Mermoz Private Hospital, Ramsay Santé (Vincent Lépilliez); ^cDepartment of Gastroenterology and Hepatology, Edouard Herriot Hospital, Hospices Civils de Lyon (Thierry Ponchon, Mathieu Pioche, Jérome Rivory); ^dDepartment of Gastroenterology, University Hospital of Rennes (Timothée Wallenhors); ^eDepartment of Gastroenterology, Hepatology, Nutrition and Digestive Oncology, University Hospital of Nantes (Emmanuel Coron, Nicolas Chapelle); ^fDepartment of Gastroenterology, Hepatology and Nutrition, Dupuytren Hospital, Limoges (Jérémie Jacques, Romain Legros); ^gDepartment of Gastroenterology and Hepatology, University Clinics of Saint Luc, Brussels, Belgium (Pierre Deprez, Enrique Perez Cuadrado Robles); ^hDepartment of Gastroenterology and Digestive Oncology, University Hospital of Bordeaux (Arthur Berger, Edouard Chabrun); ⁱDepartment of Gastroenterology and Nutrition, University Hospital of Nice (Geoffroy Vanbiervliet)

Correspondence to: Maximilien Barret, MD, PhD, Hôpital Cochin, service de gastro-entérologie et oncologie digestive, 27 Rue du Faubourg Saint Jacques, 75014, Paris, France, e-mail: maxbarret5744@yahoo.fr

Received 20 January 2026; accepted 5 April 2026; published online 26 June 2026

DOI: https://doi.org/10.20524/aog.2026.1086

Abstract

Background Endoscopic submucosal dissection (ESD) allows for en bloc endoscopic resection of T1 esophageal adenocarcinoma arising on Barrett’s esophagus (BE). Although the safety of the procedure is well established, the oncological adequacy of the procedure and the long-term follow up of the patients have not been prospectively studied.

Methods We conducted a prospective, multicenter study involving 9 French and Belgian centers. We included patients treated with ESD for a visible endoscopic lesion of more than 15mm documented with dysplasia, with a 3-year follow up. The primary endpoint was the histologically complete resection rate for adenocarcinoma and high-grade dysplasia (HGD).

Results A total of 141 patients were included in the study between December 2016 and January 2019. The R0 resection rate was 85% for adenocarcinoma and HGD, and 81% for invasive adenocarcinoma. The complication rate was 17%, of which 5% were early complications and 12% were late complications, mainly esophageal strictures. During a median follow-up length of 36.3 months, recurrence was observed in 15% of the patients and was endoscopically manageable in 44%. Eight patients (6%) underwent esophagectomy for a high-risk adenocarcinoma. Overall, 14 patients (12%) died during follow up, 3 of them (2.5%) from esophageal adenocarcinoma.

Conclusion Endoscopic resection by ESD is a safe and effective technique to treat T1 esophageal adenocarcinoma, allowing avoidance of esophagectomy in 94% of the patients.

Keywords Barrett’s esophagus, esophageal adenocarcinoma, early esophageal neoplasia, endoscopic submucosal dissection

Ann Gastroenterol 2026; 39 (5): 597-604

Patients and methods

Study population and inclusion criteria

We conducted a prospective, multicenter study including 9 centers in France and Belgium, with a 2-year enrolment period and a 3-year follow-up period. Participating centers were tertiary centers with extensive experience in ESD—at least 100 ESD procedures per operator—performed throughout the digestive tract. We included patients aged 18-90 years, with BE longer than 2 cm, and a visible endoscopic lesion of more than 15 mm, documented with dysplasia and treated by ESD. Patients with a history of endoscopic therapy for BE, thoracic radiotherapy, esophageal or gastric resection, esophageal strictures, or esophageal varices were excluded. Endoscopic evaluation was conducted in the referral center, completed by endoscopic ultrasonography and CT scan in the case of an endoscopically suspected T2 lesion (Paris 0-Is or 0-III lesion).

Endoscopic procedures

Diagnostic endoscopy was performed using a high-definition gastroscope equipped with narrow-band imaging and dual focus, or blue-laser imaging with magnification. The use of a distal attachment cap or 2% acetic acid chromoendoscopy was optional. All ESDs were performed under general anesthesia with endotracheal intubation and CO₂ insufflation. The choice of ESD knives and the techniques of resection (circumferential incision, tunnel, pocket technique, clip and line traction) was left to the operators. If more than 75% of the esophageal circumference was resected, prevention of esophageal stricture through oral steroid therapy was implemented according to the Yamaguchi protocol [10]. Long-term double-dose proton-pump inhibitors were prescribed following the procedure. Follow-up endoscopies were performed at 3 months, 12 months and 36 months, in addition to the endoscopic procedures needed for the eradication of residual BE.

The indication for additional treatment (surgery or chemoradiotherapy) after ESD was based on histopathological findings, including the presence of high-risk features, such as submucosal invasion, lymphovascular invasion, poor differentiation or positive deep resection margins.

Management decisions were discussed in multidisciplinary team meetings at each participating center, and were made on a case-by-case basis. No standardized treatment algorithm was applied across centers.

Study endpoints

The primary endpoint was the rate of histologically complete (R0) resection for adenocarcinoma and high-grade dysplasia. R0 resection was defined as lateral and deep resection margins clear of adenocarcinoma or high-grade dysplasia.

The secondary outcomes were: en bloc resection rate, R0 resection rate for adenocarcinoma, R0 resection rate for low-grade dysplasia, adverse event rate graded according to the AGREE classification [11], overall and recurrence-free survival at 1 and at 3 years, and rate of complete remission of intestinal metaplasia at 1 year and 3 years. Recurrent tumors were defined as the presence of adenocarcinoma in residual BE, termed local resection if located on the resection scar, metachronous (and local) if located on the residual BE, and distant if located in the lymph node or distant organs. We also aimed to identify factors associated with esophageal strictures, such as the circumferential extension of the resection, the preventive administration of corticosteroid therapy, and the center.

Definitions

Early recurrence was defined as recurrence detected at the first follow-up endoscopy performed at 3 months after ESD. Late recurrence was defined as recurrence detected at the 12-month follow-up endoscopy or thereafter.

High-risk adenocarcinoma was defined by the presence of at least 1 of the following features: submucosal invasion >500 μm, lymphovascular invasion, poor differentiation or positive vertical resection margin. Low-risk adenocarcinoma was defined as intramucosal or sm 1 (<500 μm infiltration of the submucosa) well differentiated adenocarcinoma, without lymphovascular invasion and with a negative vertical resection margin.

The depth of invasion for intramucosal adenocarcinoma was classified as follows: m1, limited to the lamina propria mucosae; m2, the superficial muscularis mucosae; m3, the layer in between the superficial and deep muscularis mucosae; and m4, the deep muscularis mucosae.

The depth of invasion for submucosal invasion was classified as sm1 when the depth of invasion was less than 500 μm, and sm2 when the depth of invasion was equal to or greater than 500 μm.

Statistical analysis and ethical aspects

Statistical analyses were performed using GraphPad Software (GraphPad Software Inc., San Diego, CA). Results are expressed as mean (± standard deviation) in case of a normal distribution of variables, and median (interquartile range [IQR] 25-75%) for variables with a skewed distribution, or as absolute numbers and percentages. The univariate analysis to identify factors associated with esophageal strictures was performed using Jamovi software (The jamovi project, 2024. jamovi Version 2.5 [Computer Software]. Retrieved from https://www.jamovi.org). Survival analyses were performed using the Kaplan–Meier method.

Patients’ written informed consent was obtained before their inclusion in the study. The study received approval from an Ethics Advisory Committee (Comité de Protection des Personnes CPP Île-de-France, 03/10/2016, reference Am7872-1-3340). The study was registered under the following numbers (NCT02583087 and EudraCT: 2015-004700-27).

Results

Patients’ characteristics

A total of 141 patients at 9 centers were treated with ESD for a visible lesion suspicious for neoplasia within a BE between December 2016 and January 2019. The mean number of patients per center was 15.7 (Supplementary Table 1).

The patients’ characteristics are presented in Table 1. The mean age was 68±10 years, and 89% (126/141) were men. Pre-resection biopsies indicated adenocarcinoma in 52% (74/141) of the lesions. The median follow-up time was 36.3 months (IQR 36-48.5 months). Sixteen patients were lost to follow up. The study flowchart is presented in Fig. 1.

Table 1 Patients’ characteristics

Figure 1 Flow chart of the study patients ESD, endoscopic submucosal dissection; BE, Barrett’s esophagus

Procedural characteristics

The mean procedure time was 72±43 min, the mean size of the endoscopic resection was 25±12.5 mm, and the mean duration of the hospital stay was 2.7±2 days.Thirty-eight patients received post-endoscopic stricture prevention with oral steroids. All 141 lesions in 141 patients were resected en bloc. The detailed endoscopic procedural characteristics are presented in Table 2.

Table 2 Endoscopic procedural characteristics (n=141)

Adverse events

No periprocedural perforation occurred. Sixteen (11%) periprocedural bleedings were recorded, but were not regarded as adverse events, as they were all successfully managed during the procedure with hemostatic forceps or through-the-scope clips.

There was no delayed perforation. Early (<48 h) adverse events included 2 cases of aspiration pneumonia, treated with antibiotics, and 5 delayed bleedings. Of the 5 bleedings, 3 required endoscopic hemostasis, 1 required red blood cell transfusion, while 1 patient was only admitted to the hospital for clinical and biological monitoring.

Late (>30 days) adverse events were all post-endoscopic esophageal strictures. There were 17/141 (12%) esophageal strictures, 3 among the 38 patients who had stricture prevention (3/38 patients, 8%), and 14 among the patients without stricture prevention (14/103, 14%). The univariate analysis revealed that esophageal stricture was statistically significantly associated with the proportion of esophageal circumference resected (χ²=11.2, df=1, P<0.001), but not with the use of corticosteroid therapy (χ²=0.15, df=1, P=0.698), or the treatment center (χ²=11.1, df=8, P=0.195).

According to the AGREE classification, adverse events were graded as I, II, and IIIA (mainly esophageal strictures requiring dilatation) in 1.5%, 1.5%, and 14% of patients, respectively. No grade IIIB, IV, or V adverse events were observed.

Histological analysis

Out of 141 lesions, there were 99 (70%) invasive adenocarcinomas, 31 (22%) lesions with high-grade dysplasia or in situ carcinoma, 10 (7%) lesions with low-grade dysplasia, and 1 (0.7%) hyperplastic lesion. Of the 99 adenocarcinomas, 80 (81%) had an R0 resection for invasive carcinoma. The R0 resection rate was 85% (110/130) for HGD and carcinoma and 86% (121/140) for any dysplasia and carcinoma.

Overall, there were 35/99 (36%) high-risk esophageal adenocarcinomas, and 64/99 (64%) low-risk adenocarcinomas. Other histological characteristics are presented in Table 3. Of the 35 high-risk adenocarcinomas, 17 were R0.

Table 3 Histological analysis of the resected specimens. Percentages may not sum to 100% due to rounding

Additional oncological treatments after ESD

After the initial resection, 4 patients underwent esophagectomy and 6 received chemoradiotherapy, as adjuvant or salvage treatment following histological analysis of the resection specimen. The indications for the additional treatment, follow up and status at 36 months are shown in Supplementary Table 2.

During the follow-up period, 4 additional esophagectomies, 3 chemoradiotherapies, and 3 chemotherapies were performed as treatments for cancer recurrence or as an adjuvant or salvage treatment for a cancer recurrence initially managed by ESD. In total 8 esophagectomies (6%), 9 chemoradiotherapies (6%), and 3 chemotherapies (2%) were performed.

Of the 8 esophagectomies, 3 were performed as a salvage treatment following the initial ESD in patients with R1 resection (pT1aN1, pT1bN0, pT1bN0), and 1 was performed as an adjuvant treatment for a high-risk esophageal adenocarcinoma (pT0N0). Three esophagectomies were performed for recurrent adenocarcinomas during follow up (pT1bN1, HGD, pT1aN0), and 1 was an adjuvant treatment after a second ESD performed for a local recurrence at 3 months, which had not eradicated the disease by 12 months (pT1aN2). The patient who underwent this treatment developed distant metastases by 36 months, despite the surgery, and died from esophageal adenocarcinoma.

Of the 9 chemoradiotherapy treatments, 6 were administered as adjuvant or salvage treatment following the initial ESD in patients with R1 resection or a high-risk esophageal adenocarcinoma, 2 were for recurrent adenocarcinomas, and 1 was salvage treatment after the submucosal dissection for a local cancer recurrence at 3 months, which had not eradicated the disease by 12 months.

Eradication of the residual BE

Overall, 91 (64.5%) patients received BE ablation therapy, 74 (52.5%) with radiofrequency ablation and 17 (12%) with argon plasma coagulation.

The median (IQR) size of the BE segment changed from C2 (0-7) M4 (2-8) at baseline to C0 (0-0) M0 (0-1) at 36 months. The complete remission rate of intestinal metaplasia was 64% at the end of the endoscopic follow up. Fifteen patients underwent endoscopic mucosal resection during follow up, mainly for the treatment of residual dysplastic BE, and 13 new ESDs were performed. Of these 13 ESDs, 5 showed dysplastic lesions, and 8 recurrent adenocarcinomas.

Early oncological outcomes

At 3 months, we recorded 10/141 (7%) recurrences of adenocarcinoma. Five lesions were metachronous lesions, located outside the resection area, and 5 were located on the resection scar. Of the 5 patients with a recurrence on the resection scar, 3 patients had R1 resections on the index ESD. Of these 10 recurrences, 7 were managed by a second ESD, 1 by an esophagectomy (pT1bN1), and 2 by chemoradiotherapy. Of the 7 patients treated by ESD, 4 never experienced cancer recurrence. Among the 3 remaining patients, 1 underwent surgery at 12 months for a further recurrence, developed metastases at 36 months, and died at 47 months. Another underwent chemoradiotherapy at 12 months for recurrence and died of unrelated causes at 36 months. The last patient developed metastases at 12 months, was treated with chemotherapy, and was still alive at 36 months.

Late oncological outcomes

Sixteen patients were lost to follow up, 7 were unable to continue the follow-up protocol because of another pathology (squamous cell carcinoma of the tonsil, loss of autonomy, cerebrovascular stroke, dementia), and 14 patients died, 3 from esophageal adenocarcinoma. One of these 3 patients had a high-risk adenocarcinoma, with 2 poor histoprognostic factors on the initial resection specimen, and had received adjuvant chemoradiotherapy. However, he experienced a local recurrence at 12 months that was not amenable to endoscopic resection; he received palliative treatment with an esophageal stent, and died 1 month later. The second patient had a high-risk adenocarcinoma, with 1 poor histoprognostic factor on the resection specimen, and had tumor recurrence at 3 months on the residual BE. This second lesion was treated with a second ESD, but persistent adenocarcinoma was found on the residual BE, leading to an esophagectomy. However, metastatic recurrence was diagnosed at 36 months, and the patient died 47 months after inclusion. The last patient had a high-risk adenocarcinoma with a positive vertical margin and had received adjuvant chemoradiotherapy. He died 24 months after inclusion from adverse events following esophageal stenting for a local recurrence.

Among the 17 patients with high-risk adenocarcinoma resected with R0 margins, 4 received additional oncological treatment (surgery or chemoradiotherapy). Among these patients, 2 (50%) experienced a recurrence within 3 years following resection, resulting in a 3-year recurrence-free survival rate of 50% in this group. In comparison, among the 13 patients under simple surveillance without additional treatment, 4 (31%) experienced a recurrence, resulting in a 3-year recurrence-free survival rate of 69% in this group. Overall, the 3-year recurrence-free survival rate for high-risk adenocarcinomas resected with R0 margins was 65% (11/17) in all patients, compared with 69% (9/13) in patients managed with surveillance alone and 50% (2/4) in those who received additional oncological treatment.

After a mean follow up of 39±17 months, a total of 18 esophageal cancer recurrences were recorded, including 8 late recurrences, in addition to the 10 early recurrences already observed. Among these 8 late recurrences, 1 was located at the resection scar, which was initially a high-grade dysplasia with a histologically complete endoscopic resection. Six patients presented a recurrence on the residual BE. The last patient developed a distant metastatic recurrence, consisting of a bone metastasis diagnosed at 36 months, without evidence of residual esophageal tumor at follow-up endoscopy. The initial lesion was a poorly differentiated adenocarcinoma with submucosal invasion of 160 μm, lymphovascular invasion, and a histologically complete (R0) resection. More information about the recurrent esophageal adenocarcinomas is provided in Table 4.

Table 4 Three-year follow up after endoscopic resection by ESD of an early esophageal adenocarcinoma (n=141)

Recurrence-free survival and cause-specific survival curves were generated using the Kaplan-Meier method (Fig. 2). Of the 18 recurrences, 8 were completely managed by endoscopy without the need for adjuvant or rescue treatments. Five patients required chemoradiotherapy, 4 underwent esophagectomy, and 2 received chemotherapy. The initial histological characteristics, time to recurrence, management of recurrence, and follow-up data for all recurrences are presented in Supplementary table 3.

Figure 2 Kaplan-Meier curves showing recurrence-free survival and cause-specific survival with number of patients at risk shown below the curves

Thirteen of the 18 recurrences had an initial R0 endoscopic resection. However, of these 13 recurrences, 8 were located on the residual BE, and may have corresponded to different tumors from the initial one. Of the remainder, 4 were on the scar site and 1 was a distant recurrence.

Discussion

In this study, we demonstrated that ESD achieved histologically complete resection of invasive esophageal adenocarcinoma in 81% of patients, with no procedure-related mortality and no severe adverse events. These outcomes are in line with the findings of 2 major studies on the subject (AGREE IV and V), which reported 64-100% en bloc resection rates, 62-87% rates of histologically complete resection of invasive adenocarcinoma, 72-85% for invasive adenocarcinoma, 39-65% for adenocarcinoma and high-grade dysplasia, and 0% severe adverse events [12-18]. To our knowledge, this study is the first prospective multicenter documentation of these results, confirming the feasibility, efficacy and safety of ESD for this indication.

These data question the role of surgery in the management of T1 adenocarcinoma of the esophagus. Indeed, endoscopic resection allowed esophagectomy to be avoided in 94% of patients. First, 6 of the 7 patients undergoing endoscopic surveillance, with deep R1 resection as the only risk factor for recurrence, did not have residual carcinoma at the 3-month follow-up endoscopy. This is an additional argument that the R1 factor alone may not be sufficient to suggest an additional esophagectomy, and that early endoscopic surveillance is crucial, as already suggested by others [16]. It has to be noted that none of the 3 patients with a histologically complete resection of high-risk adenocarcinoma treated with adjuvant esophagectomy presented with disease recurrence. However, the number of patients is small, and the experience of salvage esophagectomy for patients with recurrent adenocarcinoma, with 25% (1/4) cancer-related mortality, demonstrates that surgery may not be the best treatment option for aggressive disease, even at an early stage.

Considering the morbidity and mortality of esophagectomy and the 7% (11/141) mortality rate from non-adenocarcinoma-related causes in our study, the indications for additional esophagectomy after ESD of a T1 adenocarcinoma should be carefully weighed.

Besides surgery, radiotherapy or chemoradiotherapy have been proposed as adjuvant treatments following the resection of high-risk early esophageal cancer, mainly squamous cell carcinoma [19], and more rarely for adenocarcinoma [20]. Overall, 9 patients received chemoradiotherapy, 3 for high-risk adenocarcinoma, 3 for deep R1 resection and 3 for recurrent disease. Although the small patient numbers and the heterogeneity of the treatment protocols prevent the drawing of robust conclusions, only 1 of the patients who was a high-risk R0 resection at inclusion treated with chemoradiotherapy developed distant recurrence, and no severe treatment toxicity was reported.

The 3-year recurrence-free survival rate for high-risk adenocarcinomas resected with R0 margins was 65% (11/17) in all patients, compared with 69% (9/13) in patients managed with surveillance alone and 50% (2/4) in those who received additional oncological treatment. These results question the benefit of any of the currently available adjuvant treatments following endoscopic resection in terms of recurrence-free survival. The role of adjuvant immunotherapy remains to be determined in this specific clinical situation.

Paradoxically, our study brings into question the importance of R0 resection for BE associated neoplasia: first, as mentioned above and reported by others [16], deep R1 resection often did not equate to residual adenocarcinoma in the esophagus, probably because of coagulation artifacts on the resection specimen; second, 3 patients developed local recurrence of adenocarcinoma on the resection scar despite initial R0 resection, underlining the major sampling bias of any histological study; third, 11 patients had local recurrence on the residual BE, highlighting the importance of ablation of the residual BE, or at least of close endoscopic surveillance, even in frail and elderly patients.

Our work demonstrated the safety of ESD, among a large number of western centers, without any grade IV or V adverse events, and no surgery for adverse events. The most significant adverse event was esophageal stricture, recorded in 14% of patients, and requiring endoscopic balloon dilatation. Like others, we observed that a greater circumferential extent of the resection was associated with a higher likelihood of stricture [21,22]. In contrast, no significant association was observed between the use of corticosteroid therapy and esophageal stricture, indicating that corticosteroid therapy did not significantly influence the occurrence of stricture in our sample. Moreover, the analysis of hospital centers did not reveal a statistically significant association with esophageal strictures, meaning that the possibly different generator settings and different use of section or coagulation during ESD are not likely to significantly affect the rate of post-ESD esophageal strictures.

Beside the heterogeneity of the post ESD treatment protocols (esophagectomy, chemoradiotherapy, management of residual BE or recurrent lesions), and a selection bias towards more advanced lesions, the main limitation of our study lies in the 16 patients lost to follow up. A possible explanation is that these patients do not feel sick, often do not realize that they were treated for cancer, and do not understand the need to pursue endoscopic surveillance after a first normal follow-up endoscopy. This calls for better informing of patients by endoscopists about the diagnosis of early esophageal cancer and its implications. Notably, 11 of the 16 patients lost to follow up had histologically complete resection of a low-risk adenocarcinoma.

ESD allows en bloc resection of T1 esophageal adenocarcinomas in over 90% of patients, with an acceptable safety profile, allowing esophagectomy to be avoided. These results, recorded prospectively across a large number of centers and operators, justify the use of this technique to resect visible lesions larger than 15 mm suspected of cancer, or when endoscopic mucosal resection is technically impossible. Systematic ablation of BE after endoscopic resection, along with the development of adjuvant medical therapy following endoscopic resection, could reduce the rates of local and distant recurrences.

Summary Box

What is already known:

Endoscopic resection is standard for early Barrett’s neoplasia
Data on the long-term outcomes of endoscopic submucosal dissection (ESD) are limited
The safety of ESD in Barrett’s neoplasia is well established
The oncological adequacy of the procedure has yet to be studied

What the new findings are:

ESD is a safe treatment for T1 esophageal adenocarcinoma in France, allowing more than 90% of patients to avoid esophagectomy
ESD is indicated for lesions larger than 15 mm suspected of cancer
Systematic ablation of Barrett’s esophagus could reduce the rate of local recurrence

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Notes

Conflict of Interest: None